Control of Cardiac Output

Reading
Klabunde, Cardiovascular Physiology Concepts
Chapter 4 (Cardiac Function)

Basic Theory of Circulatory Function

The blood flow to each tissue of the body is almost always precisely controlled in relation to the tissue needs
The cardiac output is controlled mainly by the sum of all the local tissue flows
Frank-Starling Relationship is the predominant factor in matching venous return and cardiac output

In general, the arterial pressure is controlled independently of either local blood flow or cardiac output control

Definitions
Cardiac Output
The quantity of blood pumped into the aorta each minute

Venous Return
The quantity of blood flowing from the veins into the right atrium each minute

Cardiac Output
CO = HR x SV
SV = EDV ESV
SV EDV ESV EF EDV EDV

End-Diastolic Volume End-Systolic Volume = Stroke Volume

End-Diastolic Volume

End-Systolic Volume

Determinants of Cardiac Output

Heart Rate Preload

Cardiac Output

Contractility

Afterload

IMPORTANT RELATIONSHIPS
CONTRACTILITY (+) HEART RATE (+) CARDIAC OUTPUT PRELOAD (+) STROKE VOLUME (+) AFTERLOAD (-)

Heart Rate

Heart Rate
Changes in heart rate are generally more important quantitatively in producing changes in cardiac output than are changes in stroke volume
Changes in heart rate alone inversely affect stroke volume

Heart Rate
At low HR
Increase in HR is greater than decrement in SV

At high HR
The decrease in SV is greater than the increase in HR (decreased filling time)

Effects of Heart Rate on Cardiac Output

Cardiac Output

Heart Rate
(Increased by Pacing)

Bowditch (Treppe) Effect

An increase in heart rate will also cause positive inotropy (Bowditch effect, Treppe or staircase phenomenon).
This is due to an increase in intracellular Ca++ with a higher heart rate:
More depolarizations per minute Inability of Na+/K+-ATPase to keep up with influx of Na+, thus, the Na+-Ca++ exchange pump doesnt function as well

Factors Affecting Stroke Volume

 Stroke Volume
= EDV-ESV

End
Diastolic Volume

End
Systolic Volume

Preload

Contractility Afterload

Preload

Preload
Preload can be defined as the initial stretching of the cardiac myocytes prior to contraction. It is related to the sarcomere length at the end of diastole.
Because we cannot measure sarcomere length directly, we must use indirect indices of preload.
LVEDV (left ventricular end-diastolic volume) LVEDP (left ventricular end-diastolic pressure) PCWP (pulmonary capillary wedge pressure) CVP (central venous pressure)

Determinants of Preload
Venous Blood Pressure
Venomotor tone (Venous compliance) Venous volume
Venous Return Total Blood Volume Respiration Exercise/Muscle contraction Gravity

Filling time (Heart rate) Ventricular compliance Atrial contraction Inflow or outflow resistance Ventricular systolic failure

Frank-Starling Mechanism

Frank-Starling Mechanism
When venous return to the heart is increased, ventricular filling increases, as does preload. This stretching of the myocytes causes an increase in force generation, which enables the heart to eject the additional venous return and thereby increase stroke volume.
Simply stated: The heart pumps the blood that is returned to it

Frank-Starling Mechanism
Allows the heart to readily adapt to changes in venous return.
The Frank-Starling Mechanism plays an important role in balancing the output of the 2 ventricles. In summary: Increasing venous return and ventricular preload leads to an increase in stroke volume.

Frank-Starling Mechanism

Frank-Starling Relationship

Frank-Starling Mechanism
There is no single Frank-Starling Curve for the ventricle. Instead, there is a family of curves with each curve defined by the existing conditions of afterload and inotropy.

Frank-Starling Curves

Afterload

Afterload
Afterload can be viewed as the "load" that the heart must eject blood against.
In simple terms, the afterload is closely related to the aortic pressure.

Afterload
More precisely defined in terms of ventricular wall stress:
LaPlaces Law: Wall stress = Pr/h
P = ventricular pressure R = ventricular radius h = wall thickness

Afterload is better defined in relation to ventricular wall stress

LaPlaces Law
Wall Stress
Wall Stress

Pr h
h

P
r

Afterload
Afterload is increased by:
Increased aortic pressure Increased systemic vascular resistance Aortic valve stenosis Ventricular dilation

Effects of Afterload

Anrep Effect
An abrupt increase in afterload can cause a modest increase in inotropy.
The mechanism of the Anrep Effect is not fully understood.

Contractility

Contractility
The inherent capacity of the myocardium to contract independently of changes in afterload or preload. Changes in contractility are caused by intrinsic cellular mechanisms that regulate the interaction between actin and myosin independent of sarcomere length.
Alternate name is inotropy.

Contractility
Force of contraction
Increased rate and/or quantity of Calcium delivered to myofilaments during contraction

Heart functions at lower end-systolic volume and lower end-diastolic volume

Factors Regulating Inotropy

(+) (-)
Parasympathetic Activation Sympathetic Activation

(+)
Inotropic State
(Contractility)

Catecholamines

(+)
Afterload (Anrep)

(+)
Heart Rate (Treppe)

(-)
Systolic Failure

Ancillary Factors

Ancillary Factors Affect the Venous System and Cardiac Output

Gravity
Venous pooling may significantly reduce CO

Muscular Activity and Venous Valves

Respiratory Activity

Effects of Gravity on the Venous System and Cardiac Output

Gravity
Venous pooling may significantly reduce CO

Muscular Activity and Venous Valves

Effects of Respiration
Spontaneous respiration
Decreased intra-thoracic pressure results in a decreased right atrial pressure which enhances venous return

Mechanical ventilation
Increased intra-thoracic pressure during positive-pressure lung inflation causes increased right atrial pressure which decreases venous return

Valsalva Maneuver
Causes a large increase in intra-thoracic pressure which impedes venous return to the right atrium

Summary of Factors That Influence Cardiac Output and Mean Arterial Pressure

Myocardial Oxygen Consumption

Myocardial Oxygen Consumption

Oxygen consumption is defined as the volume of oxygen consumed per minute (usually expressed per 100 grams of tissue weight)

Myocardial Oxygen Demand is Related to Wall Stress

LaPlaces Law
Wall Stress
Wall Stress

Pr h
h

P
r

Factors Increasing Myocardial Oxygen Consumption

Increased Heart Rate Increased Inotropy (Contractility) Increased Afterload Increased Preload
Changes in preload affect myocardial oxygen consumption less than do changes in the other factors

The End